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A 43 year old male with no past medical history presented with lightheadedness. He thought the symptoms were worsened by a sour patch candy. He had no chest pain or palpitations.

His vital signs were normal. His EKG is below.

1. What does the EKG demonstrate?

2. What is the management of this condition?

ANSWER:

The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is consistent with Brugada type II.

Brugada syndrome is managed with ICD placement. There is no direct treatment for Brugada syndrome.

The EKG shows high take off ST elevations in leads V1 and V2 with a gradually descending ST segment. This is sometimes referred to as a “saddle back configuration”. This is consistent with Brugada type II.

Brugada syndrome is a genetic (autosomal dominant) sodium channel defect. It predominantly affects males (90%). Patients with Brugada syndrome are at risk for polymorphic V-tach. Patients who had a syncopal or near-syncopal episode who have an EKG pattern consistent with Brugada syndrome must be suspected of having had an episode of V-tach.

Brugada type I presents with downsloping, or “coved”, ST elevations in leads V1 and V2 leading into inverted T waves. There is no isoelectric separation between the QRS complex and the T wave.

There is no specific treatment for Brugada syndrome. So, these patients require placement of an ICD to manage their ventricular arrhythmias.

Our patient went to the EP lab and the diagnosis of Brugada was confirmed. He had an ICD placed and is doing well. The sour patch candy was likely a red herring.

The bundle branch block went away. This is known as a rate related bundle branch block.

The first EKG shows rapid a-fib with a left bundle branch block. The patient was treated with diltiazem with resultant control of the heart rate. When that happened the bundle branch block disappeared and the QRS narrowed. This is known as a rate related bundle branch block.

As the heart rate increases, the cardiac cycle shortens. Eventually the next beat arrives when one bundle is still refractory. So it conducts down the other bundle and then across the heart, the same as in a regular bundle branch block. However, when the heart rate slows, the cardiac cycle lengthens and the bundle recovers. When the bundle recovers the bundle branch block disappears.

No specific treatment is needed for a rate-related bundle branch block.

A 59 y/o male with no significant past medical history presented to the ED complaining of weakness and shortness of breath. He had been fatigued for several weeks. He presents drowsy.

V/S: Pulse 120, Respirations 28, BP 180/90.

His EKG is below.

What does the EKG demonstrate?

How would you manage this patient?

ANSWER:

The EKG shows a wide QRS complex with an irregular rhythm.

This EKG is concerning for hyperkalemia. This patient’s Potassium was 9.9. He was treated with calcium, insulin, glucose, albuterol, bicarb and emergent dialysis.

Hyperkalemia causes a series of changes to the EKG. An early sign is peaked T waves. This is followed by flattening of P waves, widening of the QRS complex and ultimately a sine wave. Whenever you see a wide QRS complex with a bizarre rhythm or what looks like “slow V-tach”, think about hyperkalemia.

This patient was given calcium. The repeat EKG below shows some improvement in the rhythm but the QRS remained wide.

The patient was found to have AKI with BUN 225 and Cr 25. Blood gas showed pH 6.95, pCO2 16, HCO3 4. A foley was placed and the patient was anuric.

The patient was sent for emergent dialysis. After dialysis the EKG (below) shows a normal sinus rhythm with a narrow QRS complex.

59 year old male with a history of hypertension and high cholesterol, presented to an urgent care center complaining of chest pain. The pain began 48 hours prior as a substernal burning sensation radiating to bilateral arms occurring at rest. The day before presentation the pain recurred with minimal exertion.Family history significant for father who died at age 58 from an MI.

The EKG is below.

1. What does the EKG demonstrate?

2. What is the significance of these findings?

3. How would you manage this patient?

ANSWER:

The EKG shows biphasic T waves in leads V1-V3 extending out to V6.

This is known as Wellen’s sign. It suggests a critical proximal LAD occlusion.

The patient should receive aspirin and other anti-platelet therapy (clopidogrel or ticagrelor). He should be sent to an Emergency Department with emergent cardiology consult for possible cath.

The EKG shows a sinus rhythm with biphasic T waves in leads V1-V3 extending out to V6. This pattern is known as Wellen’s sign. It is suggestive of a proximal LAD occlusion and a 75% risk of anterior wall MI. Wellen’s sign consists of a minimally elevated takeoff of the ST segment from the QRS complex, a concave or straight ST segment and a symmetrically inverted T wave in leads V1-V3. Some patients can have findings extend out to lead V4 or even V5 and V6. (de Zwaan et al. Characteristic Electrocardiographic Pattern Indicating a Critical Stenosis High in LAD in Patients Admitted Because of Impending Myocardial Infarction. Am Heart J 1982;103:730-6.)

Our patient was transferred to the ED. His initial troponin was 1.63. Cardiac cath showed a 99% occlusion of the proximal LAD.

Our patient reported pain radiating down both arms. Classically, MI’s are described as presenting with chest pressure radiating down the left arm. However, the literature suggests that pain radiating down the right arm is equally suggestive of acute coronary syndrome as the left arm. Radiation to both arms is the most predictive. (Fanaroff et al. Does This Patient With Chest Pain Have Acute Coronary Syndrome?: The Rational Clinical Examination Systematic Review. JAMA. 2015 Nov 10;314(18):1955-65.)

A 56 year old male with a history of multiple myeloma and cardiac amyloidosis complains of palpitations. Vital signs: Pulse 180, Respirations 18, BP 140/80. His EKG is below.

1. What is the rhythm in this EKG?

2. How would you manage this patient?

ANSWER:

The rhythm is atrial fibrillation with a rapid ventricular response

The patient is hemodynamically stable so he can be managed medically with rate control using AV nodal blockers such as diltiazem.

The EKG demonstrates a tachycardia (rate ~180) with a narrow QRS complex and an irregular rhythm with absent P waves and the presence of fibrillatory waves. This is consistent with atrial fibrillation.

Patients with rapid a-fib who are hemodynamically unstable, and the instability is due to the tachycardia, should be treated with electrical synchronized cardioversion.

Patients who are hemodynamically stable can be treated medically. First line treatment includes calcium channel blockers (such as diltiazem) or beta blockers. Second line treatment includes amiodarone and digoxin.

Our patient had a history of cardiac amyloidosis. In general, beta blockers and calcium channel blockers should be avoided in patients with cardiac amyloidosis because they can cause worsening of heart failure. So, our patient was initially treated with amiodarone. This was unsuccessful, so the patient was electrically cardioverted. His post-cardioversion EKG is below. It demonstrates a sinus rhythm with lateral ST depressions.

The EKG demonstrates ST elevations in leads II, III and AVF with reciprocal depressions in V2-V6, I and aVL. This is consistent with an inferior wall (or inferoposterior) STEMI.

The rhythm is sinus with a 2nd degree 2:1 AV block.

The MI should initially be treated with antiplatelet drugs (aspirin, clopidogrel/prasugrel). The bradycardia with AV block should be treated with a pacemaker, as the patient is hypotensive. Initially, a transcutaneous pacer should be placed followed by a transvenous pacer. Once appropriate capture is obtained and the heart rate normalizes, the patient should go to the cath lab for emergent PCI.

ST elevations are a sign of acute MI. When you identify both ST depressions and ST elevations on the same EKG, that represents an acute MI in the area of the ST elevations. The ST depressions in that case are only reciprocal changes. Leads II, III and aVF look at the inferior wall of the heart.

Inferior wall MI’s can be associated with bradycardia and AV block. This EKG demonstrates bradycardia with dropped P waves. Some of the P waves are conducted through and some are not (best seen in lead V1). That is characteristic of 2nd degree AV block. Differentiating 2nd degree AV block from 3rd degree AV block can sometimes be difficult, as in this EKG. The following algorithm may be helpful. In this EKG, the RR intervals are regular and the PR intervals are regular. So, we are dealing with 2nd degree AV block.

2nd degree AV block comes in two types – type I (AKA Mobitz I, Wenckebach) and type II (AKA Mobitz II). In type I, the PR intervals progressively lengthen followed by a dropped P wave. Then the PR interval shortens again and the cycle repeats. In type II, all PR intervals are the same and there are some dropped P Waves. To differentiate 2nd degree type I from type II, you must see two consecutive beats where the sinus impulse conducts through. This allows you to determine if the PR interval is progressing (type I) or not (type II). In our EKG, every second sinus beat is dropped (best seen in lead V1). So, you do not see two consecutive sinus beats conducting through. This prevents you from differentiating 2nd degree type I from 2nd degree type II. This EKG pattern is referred to as a 2:1 AV block (every second beat is blocked by the AV node). In general, in 2:1 AV block, the presence of a prolonged PR interval makes type I block more likely, whereas the presence of wide QRS complexes makes type II block more likely. However, this is not entirely reliable.

When faced with a 2:1 AV block, running a long rhythm strip may allow you to see two consecutive conducted beats. You can then measure consecutive PR intervals to see if they are prolonging (type I) or the same (type II).

An 83 year old female with a history of COPD and CAD presents to the ED with a brief episode of right sided CP associated with palpitations. Patient denies syncope. No nausea, vomiting. No SOB.

Vital signs: Pulse – 80, R – 18, BP - 144/92, O2 sat 98%.

Her EKG is below.

1. What is the rhythm?

2. How would you manage this patient?

ANSWER:

The rhtyhm is sinus rhythm with non-conducted PAC’s

Non-conducted PAC’s are treated the same as patients with PAC’s – look for a cause, check electrolytes, usually no emergent intervention needed.

The EKG demonstrates a sinus rhythm at a rate of approximately 80. After beats #4, 7 and 11, there are P waves with no QRS complex following them (See below). However this is NOT 2nd degree AV block.

If you map out the P waves, the “dropped” P waves come earlier than expected. In fact, they come right after the preceding T wave. Since the P waves come so early, the ventricles are still refractory so they do not conduct.

The way we know this is not AV block is because the P waves come earlier than expected. This patient needs no emergent intervention and should not have a pacemaker placed.

Non-conducted PAC’s may appear like a 2o AV block. You see P waves with no QRS complex following them and a pause on the rhythm strip. However, to call something 2o AV block, the P waves must come on time (i.e. the P-P interval must be regular). So, whenever you diagnose AV block, measure the P-P intervals and make sure they are regular. If the “dropped” P wave comes early, it is likely a non-conducted PAC and not AV block.

Non-conducted PAC’s are a very common cause of pauses on EKG. Whenever you encounter a pause, look back at the preceding T wave before the pause to see if there is a P wave buried in there.

Pauses on EKG can be caused by 3 things: Non-conducted PAC’s, SA node disease (SA block and SA arrest), and AV block. The following algorithm may be useful to diagnose pauses: